Air trapping causes a Ca2(+)-channel-mediated increase in pulmonary vascular resistance in neonatal lambs.

Air trapping and alveolar hyperinflation may occur during mechanical ventilation in the presence of severe airway obstruction, during fast ventilator rates, and when expiratory time is compromised. Inadvertent positive end-expiratory pressure may occur with air trapping and increased mean airway pressure. The pulmonary artery pressure response to air trapping, produced during volume-regulated time-cycled ventilation, was studied in neonatal lamb lungs, isolated in situ, and perfused at a constant flow rate (50-75 ml.kg-1.min-1), both before and after Ca2(+)-channel blockade with verapamil (5 mg). The hub of the endotracheal tube was narrowed to a 1.5-mm orifice to produce fixed proximal airway obstruction. Air trapping was then produced by lengthening inspiratory time from 25 to 80%, at zero end-expiratory pressure. The magnitude of inadvertent positive end-expiratory pressure due to air trapping was estimated by end-expiratory occlusion pressure. End-expiratory occlusion pressure was 0.20 +/- 0.03 kPa (1.7 +/- 0.2 mm Hg) and 1.60 +/- 0.01 kPa (11.8 +/- 1.0 mm Hg), at 25 and 80% inspiratory times, respectively. On lengthening inspiratory time, mean pulmonary artery pressure (mPpa) increased briskly within 30 s followed by a gradual increase over the next 4 min. Verapamil blunted both the brisk and the gradual increase in mPpa on lengthening inspiratory time. Lengthening inspiratory time increased the mPpa by 2.0 +/- 0.1 kPa (14.7 +/- 0.8 mm Hg) from baseline, and verapamil reduced this increase to 1.3 +/- 0.1 kPa (10.1 +/- 0.6 mm Hg; p less than 0.05 by analysis of variance).(ABSTRACT TRUNCATED AT 250 WORDS)